The goal of this research proposal is to investigate the effect of plasma homocysteine concentrations on changes in the circulating concentrations of cellular fibronectin (CFN), a marker of endothelial dysfunction. Increased concentrations of plasma homocysteine have been found to be a strong independent risk factor for stroke, coronary and peripheral vascular disease. The mechanism by which increased plasma homocysteine promotes vascular disease is unknown, however homocysteine is thought to exert a direct cytotoxic effect upon the function of endothelial cells. Plasma homocysteine concentrations from fasting individuals have been found to correlate strongly with CFN, a marker of endothelial dysfunction. These results have led to following hypothesis: Homocysteine has an effect upon endothelial cell function that leads to an increased release of cellular fibronectin as a marker of endothelial dysfunction. The specific aim is to demonstrate whether increases in plasma homocysteine concentrations are associated with endothelial cell function as assessed by increases in the release of cellular fibronectin.